Human T-cell Leukemia disease type 1 (HTLV-1) is a retrovirus of oncogenic nature that is competent at its role to cause life-threatening diseases in the human population, for instance, a powerful lethal condition termed Adult T-cell Leukemia/Lymphoma (ATLL) and more occasionally neurological condition termed as Tropical Spastic Paraparesis (TSP) which is also termed as HTLV-associated Myelopathy (HAM). Experts give an estimation of ten-twenty million persons impacted by HTLV-1 intercontinental. The epidemiology that is poorly understood, the unavailability of vaccines and the absence of targeted anti-retroviral treatment have compelled the Global virus network to dispatch a task group in the year 2014. They focussed mainly on the enhancement of various possible procedures for the clinical management (examination and treatment) of the people infected with HTLV-1. HTLV-1 Transmission at a cellular level is achieved via contact of one cell with another and generation of plenty of infected cesses so that it can hang on there and accomplish transmission of infection to another vulnerable host. Viral propagation through cell-to-cell contacts leads to the enhancement of a load of the provirus. The enhanced load of the provirus is a significant factor allied with the progression of ATLL and other inflammation-associated diseases. The tax and HTLV-1 bZIP factor (HBZ) are the virally encoded genes that through their accommodating actions accomplish variation of the immunophenotype of infected cells, induction of proliferation and apoptotic inhibition of the cells to enhance the number of infected cells. Subsequently, infected cells hang tight, multiply and infiltrate into the tissues, which is probably the key factor for the transmission of HTLV-1. Both kinds of HBZ (protein and mRNA) play a crucial role in the oncogenesis of HTLV-1. The structural configuration of HBZ protein (shape) with its relationship with host cell proteins, for instance, p300-CBP, Foxo3a as well as Foxp3 execute different key roles (apoptotic process, proliferation augmentation, and anti-viral activity weakening) so as to modify transcription profile of T-cells and thus provoking the development of oncogenesis. The current article is basically occupied with determining the initiation of HTLV-1 infection, the strategy of cellular transmission, disease development at a molecular level and related prophylaxis and treatment.